Microarray analysis of choline-deficient L-amino acid-defined (CDAA) diet-induced NAFLD animal model.
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ABSTRACT:
PROVIDER: PRJNA946703 | ENA |
REPOSITORIES: ENA
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Project description:Nonalcoholic Fatty Liver Disease (NAFLD) is a broad spectrum of liver disorders ranging from simple steatosis to nonalcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma. The choline-deficient L-amino acid-defined (CDAA) diet-induced NAFLD animal model has traditionally been used to understand the molecular mechanisms of disease development and progression. Although this animal model shows a similar course of disease progression to human NAFLD, it does not develop comorbidities such as obesity and type 2 diabetes. Therefore, its relevance to human NAFLD (what aspects of the disease etiology are recapitulated in this model?) is not fully understood. We applied microarray analysis to characterize its pathophysiology, and evaluate the similarity across species.
2023-03-25 | GSE227714 | GEO
Project description:Choline and methionine/choline deficient diets are widely used to generate severe rodent hepatic steatosis and steatohepatitis in an attempt to reflect stages of human non-alcoholic fatty liver disease (NAFLD). The underlying mechanism of hepatic injury in these models, and how this reflects human disease remains incompletely understood. We used detailed transcriptional analysis to interrogate the molecular mechanisms of this intervention and its similarity to human disease. Adult C57Bl/6J mice were maintained on control, choline deficient (CDD) or methionine/choline deficient (MCDD) diets for 4 weeks. Isolated liver RNA was used for transcriptional profiling by micro array analysis.
2016-06-01 | E-MTAB-3943 | biostudies-arrayexpress
Project description:Nucleotide signaling pathways are found in all kingdoms of life and are utilized to coordinate a rapid response to changes in the environment. One more recently discovered signaling nucleotide is the secondary messenger cyclic diadenosine monophosphate (c-di-AMP), which is widely distributed among bacteria and is also found in several archaea. This cyclic nucleotide has been shown to involve in several important cellular processes, including maintenance of DNA integrity, cell wall metabolism, stress tolerance, transcription regulation and virulence. However, the mechanisms by which c-di-AMP modulates these physiological changes have remained largely unknown.In the present study, we identified and characterized a c-di-AMP synthase (CdaA) in S. mutans UA159. Furthermore, we investigated the role of CdaA in S. mutans cell physiology and global gene expression by utilizing cdaA gene in-frame deletion mutant. Our findings suggest that CdaA is an important global modulator of optimal growth and environmental adaption in this pathogen. Streptococcus mutans UA159 whole-genome arrays (8 x 15 K) were obtained from Agilent and included 1998 probes for S. mutans transcripts. For microarray analysis, S. mutans UA159 and S. mutans ?cdaA cells were routinely grown at 37°C anaerobically (90% N2, 5% CO2, 5% H2) in brain heart infusion broth (BHI; Difco, Sparks, MD, USA) to an optical density at 600 nm (OD600) of 0.5. Four RNA samples isolated from four independent cultures of UA159 and cdaA mutant strains were hybridized to the arrays and analyzed.
2015-04-06 | E-GEOD-65511 | biostudies-arrayexpress
Project description:Transcriptomic profiles of wild type and TSP1 knockout mice that were fed control (normal) diet or CDAHFD (choline deficient amino acid defiend high fat diet) chow for 12 weeks to model Non-alcoholic Steatohepatitis (NASH) disease in humans.
2019-05-31 | GSE120977 | GEO
Project description:Nucleotide signaling pathways are found in all kingdoms of life and are utilized to coordinate a rapid response to changes in the environment. One more recently discovered signaling nucleotide is the secondary messenger cyclic diadenosine monophosphate (c-di-AMP), which is widely distributed among bacteria and is also found in several archaea. This cyclic nucleotide has been shown to involve in several important cellular processes, including maintenance of DNA integrity, cell wall metabolism, stress tolerance, transcription regulation and virulence. However, the mechanisms by which c-di-AMP modulates these physiological changes have remained largely unknown.In the present study, we identified and characterized a c-di-AMP synthase (CdaA) in S. mutans UA159. Furthermore, we investigated the role of CdaA in S. mutans cell physiology and global gene expression by utilizing cdaA gene in-frame deletion mutant. Our findings suggest that CdaA is an important global modulator of optimal growth and environmental adaption in this pathogen.
2015-04-06 | GSE65511 | GEO
Project description:We perform RNAseq in NAFLD livers from WT and miR-33-AlbCRE conditional knock-out mice. Liver were isolated from mice after 3 months of feeding a choline deficient high fat diet to analyze the effect of miR-33 deficiency.
2024-10-01 | GSE220093 | GEO
Project description:The aim of the study was to analyze the impact of choline intake during pregnancy and/or lactation on histological alternation and gene expression profile in the liver of NAFLD dam progeny. We hypothesized that offspring of mothers suffering from non-alcoholic fatty liver (NAFLD) is more prone to develop fatty liver, because of suboptimal intrauterine environment. The performed analyses included histological examination of liver tissue obtained from 24-day-old male rats, which were offspring of dams with fatty liver: provided with proper choline amount during pregnancy and lactation (NN), fed a choline-deficient diet during these both periods (DD), deprived with choline only during pregnancy (DN) or only during lactation (ND). The global gene expression profile was analyzed by using microarray approach (Affymetrix® Rat Gene 2.1 ST Array Strip).
2024-05-20 | GSE225805 | GEO
Project description:Despite recent advancements in melanoma therapy, hepatic metastasis in malignant melanoma patients remains associated with significantly reduced overall survival rates. Given the rising prevalence of metabolic liver diseases such as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NAFLD/NASH), we investigated whether metabolic changes influence hepatic melanoma metastasis. Our study found that induction of advanced NASH in C57BL/6N mice through a choline-deficient L-amino acid (CDAA)-defined diet for ten weeks significantly increased hepatic metastasis, as demonstrated by injecting B16F10Luc2 and Wt31 melanoma cells. B16F10Luc2 cells showed heightened metastatic potential even with shorter periods of CDAA feeding before liver fibrosis developed. Conversely, hepatic steatosis induced by a high-fat diet alone did not promote increased melanoma metastasis. Early pre-fibrotic changes in the hepatic vascular niche, particularly in liver sinusoidal endothelial cells (LSECs), appeared to be responsible for the enhanced metastasis, characterized by continuous endothelial dedifferentiation and upregulation of adhesion molecules VCAM1, ICAM1, and E-selectin. Functionally, B16F10Luc2 cell retention in the hepatic vascular niche was significantly increased early after CDAA feeding, with ICAM1 inhibition leading to a notable reduction in cell retention. In summary, our findings highlight the hepatic vascular niche's sensitivity to metabolic alterations, suggesting potential avenues for preventing hepatic melanoma metastasis through angiotargeted therapies.
2025-02-05 | GSE264318 | GEO
Project description:Despite recent advancements in melanoma therapy, hepatic metastasis in malignant melanoma patients remains associated with significantly reduced overall survival rates. Given the rising prevalence of metabolic liver diseases such as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NAFLD/NASH), we investigated whether metabolic changes influence hepatic melanoma metastasis. Our study found that induction of advanced NASH in C57BL/6N mice through a choline-deficient L-amino acid (CDAA)-defined diet for ten weeks significantly increased hepatic metastasis, as demonstrated by injecting B16F10Luc2 and Wt31 melanoma cells. B16F10Luc2 cells showed heightened metastatic potential even with shorter periods of CDAA feeding before liver fibrosis developed. Conversely, hepatic steatosis induced by a high-fat diet alone did not promote increased melanoma metastasis. Early pre-fibrotic changes in the hepatic vascular niche, particularly in liver sinusoidal endothelial cells (LSECs), appeared to be responsible for the enhanced metastasis, characterized by continuous endothelial dedifferentiation and upregulation of adhesion molecules VCAM1, ICAM1, and E-selectin. Functionally, B16F10Luc2 cell retention in the hepatic vascular niche was significantly increased early after CDAA feeding, with ICAM1 inhibition leading to a notable reduction in cell retention. In summary, our findings highlight the hepatic vascular niche's sensitivity to metabolic alterations, suggesting potential avenues for preventing hepatic melanoma metastasis through angiotargeted therapies.
2025-02-05 | GSE264254 | GEO
Project description:Despite recent advancements in melanoma therapy, hepatic metastasis in malignant melanoma patients remains associated with significantly reduced overall survival rates. Given the rising prevalence of metabolic liver diseases such as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NAFLD/NASH), we investigated whether metabolic changes influence hepatic melanoma metastasis. Our study found that induction of advanced NASH in C57BL/6N mice through a choline-deficient L-amino acid (CDAA)-defined diet for ten weeks significantly increased hepatic metastasis, as demonstrated by injecting B16F10Luc2 and Wt31 melanoma cells. B16F10Luc2 cells showed heightened metastatic potential even with shorter periods of CDAA feeding before liver fibrosis developed. Conversely, hepatic steatosis induced by a high-fat diet alone did not promote increased melanoma metastasis. Early pre-fibrotic changes in the hepatic vascular niche, particularly in liver sinusoidal endothelial cells (LSECs), appeared to be responsible for the enhanced metastasis, characterized by continuous endothelial dedifferentiation and upregulation of adhesion molecules VCAM1, ICAM1, and E-selectin. Functionally, B16F10Luc2 cell retention in the hepatic vascular niche was significantly increased early after CDAA feeding, with ICAM1 inhibition leading to a notable reduction in cell retention. In summary, our findings highlight the hepatic vascular niche's sensitivity to metabolic alterations, suggesting potential avenues for preventing hepatic melanoma metastasis through angiotargeted therapies.
2025-02-05 | GSE264249 | GEO